Premedication with dexmedetomidine forprevention of hyperdynamic response afterelectroconvulsive therapy: a cross-over,randomized controlled trialPattika Subsoontorn1, Varinee Lekprasert1, Punjaporn Waleeprakhon2, Pichai Ittasakul2*, Atchaporn Laopuangsak1 andSuwimon Limpoon1
Abstract
Background: Electroconvulsive therapy (ECT) is an effective therapy for psychiatric disorders, but is associated withacute hyperdynamic responses including transient hypertension and tachycardia. This study aimed to assess theeffectiveness of premedication with dexmedetomidine for hemodynamic attenuation after ECT and to evaluate itseffects on seizure duration, postictal asystole duration, post ECT agitation and recovery time.
Methods: Twenty-four psychiatric patients who underwent a total of 72 ECT sessions (three sessions per patient)were randomly allocated to receive either dexmedetomidine 0.5 mcg/kg intravenous, dexmedetomidine 1 mcg/kgintravenous, or saline (control group) 15 min before the first ECT session. The patients subsequently received theother two premedication options for their next two ECT sessions. Blood pressure and heart rate were recorded at 5,10, and 15 min after drug infusion and at 2.5, 5, 7.5, 10, 15, 20, 25, and 30 min after ECT. Asystole duration, seizureduration, post ECT agitation and recovery times were also recorded.
Results: The baseline characteristics were similar between the groups. Systolic blood pressure in bothdexmedetomidine groups was significantly lower than that in the control group after ECT (p = 0.002). Diastolicblood pressure and heart rate were significantly lower in the dexmedetomidine 1 mcg/kg group (p = 0.002 and p =0.013, respectively) compared with the control group. Asystole duration, seizure durations, post ECT agitation andrecovery times were similar between the groups.
Conclusions: Dexmedetomidine 1 mcg/kg administered 15 min before ECT attenuated the hemodynamicresponse, including suppressing the systolic, diastolic and heart rate increases, during ECT without affectingrecovery time. It also did not prolong the post-stimulus asystole duration.
Trial registration: TCTR20170715003, registered at Thai Clinical Trials Registry (TCTR), principal investigator: PattikaSubsoontorn, date of registration: 15/07/2017.
* Correspondence: [email protected] of Psychiatry, Faculty of Medicine Ramathibodi Hospital,Mahidol University, 270 Rama VI Road, Rachathewi, Bangkok 10400, ThailandFull list of author information is available at the end of the article
Subsoontorn et al. BMC Psychiatry (2021) 21:408 https://doi.org/10.1186/s12888-021-03406-9
BackgroundElectroconvulsive therapy (ECT) is an effective therapyfor psychiatric disorders in patients who have notresponded to pharmacotherapy. In ECT, a generalizedseizure is induced by a brief unilateral or bilateral elec-trical stimulus. ECT causes generalized autonomic ner-vous system stimulation, initially producing bradycardiainduced by parasympathetic nerve stimulation, followedimmediately by more prominent sympathetic stimulationthat results in transient tachycardia and hypertension[1]. The acute hyperdynamic response may be harmfulto patients with ischemic heart diseases, hypertensionand cerebrovascular disease [2, 3].Many drugs, such as α-2 adrenergic agonists, β-
blockers and opioids, have been used to attenuate theacute hemodynamic responses typically induced by theECT stimulus [4–7]. Alpha-2 adrenergic agonists de-crease stress-induced sympathetic responses to improveintraoperative hemodynamic stability [8]. Dexmedetomi-dine is a highly selective α-2 adrenergic agonist. Itinhibits central sympathetic outflow at presynaptic re-ceptors and reduces peripheral norepinephrine release[9]. A previous meta-analysis reported reductions inmorbidity and mortality associated with various types ofsurgery when patients were treated with dexmedetomi-dine [10]. Some studies showed attenuation effect ofdexmedetomidine for premedication before ECT butsome did not. This may be due to differences in dexme-detomidine dose and anesthetic regimen used duringECT [4–6, 11, 12]. This study aimed to evaluate the ef-fect of dexmedetomidine (0.5 mcg/kg and 1 mcg/kg) onthe hyperdynamic response after ECT and to evaluatethe effect on seizure duration, postictal asystole duration,post-ECT agitation and recovery time.
MethodsThis study was a crossover, double-blind randomizedcontrolled trial conducted during May 2017 to April2018 in Ramathibodi Hospital, Mahidol University,Thailand. The study participants were selected from pa-tients recommended for ECT by a psychiatrist, and whowere between 18 to 70 years old with an American Soci-ety of Anesthesiologist (ASA) physical status of I–III.The exclusion criteria were patients with liver disease,severe ventricular dysfunction, advanced heart block, oran allergy to the study drugs, or who were currentlypregnant or using any β-blockers or narcotics. Informedconsent was obtained from all eligible patients, or fromrelatives of patients who were unable to make an in-formed decision, before enrollment in the study.After obtaining approval from Ramathibodi Ethics
Committee (ID 02–60-15), the study was registered beforeparticipant recruitment with Thai Clinical Trials Registry(https://www.thaiclinicaltrials.org/). The registration
number is TCTR20170715003, date of registration: 15/07/2017. The sample size was calculated from a previous study[5] to detect a 25% difference in hemodynamic values. Apower analysis was performed with a power of 0.8 andsignificance level of 0.05, and a sample size of 24 patientswas required to reach the primary study endpoint.The primary outcomes were post-ECT blood pressure
and heart rate (HR). The secondary outcomes were inci-dence of post-ECT agitation, seizure duration (motorand EEG), asystole duration (post-ictal and post-stimulus) and recovery time. The asystole duration wasdetermined by the absence of ventricular contraction de-tected on an electrocardiogram. Patients enrolled in thestudy were randomly assigned by computer-generatedrandom numbers to receive one of three premedicationsthat were given 15min before their first ECT session.The patients subsequently received the other two pre-medication options for their next two ECT sessions.After randomization, sequence pattern for each patientwould be enclosed in envelope. Patients were blindedfrom the study drugs. The drug solutions were preparedby an anesthesiologist who was involved in the study,but administration was performed by an anesthetic nursewho was blinded to the study drugs.Each patient was evaluated by an anesthesiology resi-
dent before the procedure. Baseline characteristics of thepatients, including name, height, weight, comorbidities,current medication and ASA physical status, were re-corded. If the patient was on antihypertensive medica-tion, it was continued as usual before the ECT. Afterstandard monitoring, patients in group A received dex-medetomidine 0.5 mcg/kg, patients in group B receiveddexmedetomidine 1 mcg/kg and patients in the controlgroup received saline. All solutions were prepared in atotal volume of 25 mL and given by intravenous (IV) in-fusion over 15 min. Arterial blood pressure and HR wererecorded immediately before, and at 5, 10 and 15minafter starting the drug infusion.Immediately after the drug infusion was completed,
anesthesia was induced with thiopental 2–3 mg/kg orpropofol 1–2 mg/kg. The total dose of propofol or thio-pental that each patient received was recorded. Afterloss of consciousness, a pneumatic tourniquet was ap-plied to one leg and inflated to isolate the leg circulationand allow for an accurate assessment of the motor seiz-ure. Succinylcholine (1–2 mg/kg, IV) was then adminis-tered and ventilation was assisted with 100% oxygen inall patients. When paralysis was achieved, the electricalstimulus was applied. After cessation of the EEG andclinical motor seizure, manual ventilation was initiateduntil the patient’s spontaneous breathing was sufficientand the airway was patent. Patients were then trans-ferred to the postanesthesia care unit and monitoringwas continued.
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Arterial blood pressure and HR were recorded imme-diately after ECT and then in 2.5-min intervals up to 10min, then 5-min intervals up to 30 min. Through treat-ment session, acceptable blood pressure and heart ratewere defined as within 20% lower or higher than eachpatient baseline (immediately before start premedica-tion). If unacceptable blood pressure or heart rate persistlonger than 5min, in-charged anesthesiologist wouldgive treatment as appropriate. The duration of EEG seiz-ure, motor seizure and asystole were recorded. The re-covery time was recorded as the time from the end ofsuccinylcholine administration until the patient wasobeying commands. The agitation degree was evaluatedby a postanesthetic care nurse using a postictal agitation4-point numeric rating scale (1 = calm or asleep, 2 = rest-less but calmed down when talked to, 3 = restless and re-quired a nurse to stand next to the bed, 4 = one or morenurses were required to physically hold down the pa-tient). The CONSORT diagram is shown in Fig. 1.
Statistical analysisNominal data, such presence of underlying diseases,were summarized as number and percentage of patients.
Continuous data, such as age and blood pressure, weresummarized as mean ± standard deviation (SD), or me-dian and interquartile range (IQR) based on normality ofthe distribution. Group comparisons were performedusing a chi-square test (Fisher’s or Monte Carlo) for cat-egorical variables and one-way ANOVA or the Kruskal–Wallis test for continuous variables. For repeated mea-surements and subsequent post hoc tests for systolicblood pressure, diastolic blood pressure and HR, the re-peated measures ANOVA was used. The p-values wereBonferroni-adjusted (alpha level = 0.05/3 = 0.0167) withtime as a within-group variable. SPSS 20.0 (IBM Corp.,released 2011, IBM SPSS Statistics for Windows, Version20.0. Armonk, NY) was used for statistical analysis. A p-value less than 0.05 was considered statisticallysignificant.
ResultsThe study included 10 male and 14 female participants.The recruitment and data collection were between July2017 to February 2018. In total, 72 ECT sessions wereevaluated from three separate treatment sessions per pa-tient. No participants were excluded from the study due
Fig. 1 CONSORT flow diagram
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to exclusion criteria. Baseline characteristics were shownin Table 1. There were no differences in patient charac-teristics between the groups. Systolic and diastolic bloodpressures at baseline, after drug administration, and afterECT were shown in Fig. 2.After administration of dexmedetomidine, systolic
blood pressure of all groups was decreased from baselinewithin 15min. However, the values were still within theacceptable range. Systolic blood pressure measurementsin both dexmedetomidine groups were significantlylower than those in the control group at all time pointsafter ECT (p = 0.002). Post hoc analysis indicated a sig-nificant difference for both the dexmedetomidine 0.5mcg/kg group (p = 0.012; mean difference, − 12.27; 95%CI [− 22.41, − 2.12]) and dexmedetomidine 1 mcg/kggroup (p = 0.003; mean difference, − 14.31; 95% CI [−24.46, − 4.17]). The peak systolic blood pressure oc-curred at 5 min after ECT, and the dexmedetomidine 1mcg/kg group had the lowest measurement at this timepoint (Control, 157.33 ± 28.94; Group A, 144.04 ± 30.11;Group B 142.08 ± 25.87).Diastolic blood pressure was significantly lower in the
dexmedetomidine groups compared with the controlgroup (p = 0.016). Post hoc analysis indicated that dia-stolic blood pressure was significantly lower in only thedexmedetomidine 1 mcg/kg group compared with con-trol group at all time points after ECT (p = 0.002; meandifference, − 7.55; 95% CI [− 14.19, − 0.91]).HR measurements after drug administration and ECT
were shown in Fig. 3. Fifteen minutes after drug admin-istration, HR of all groups decreased from baseline butwas still higher than 70 beat/min. After ECT, HR signifi-cantly differed between the three groups (p = 0.012).However, when comparing between the groups, the onlysignificant differences were between the dexmedetomi-dine 1 mcg/kg group and control group at all timepoints after ECT (p = 0.013; mean difference, − 14.71;95% CI [− 26.98, − 2.44]). The carry-over effect was
minimized by adequate washout period at least 24 hinterval between each premedication drug before eachECT session. The carry-over covariates (period of meas-urement 1–3) were drop and re-run the repeated mea-sures ANOVA for systolic, diastolic blood pressure andheart rate to check if there was significant carry-over ef-fect. The results yielded no significant (p > 0.05).Secondary outcomes were shown in Table 2. Recovery
time, EEG seizure duration, asystole duration and agita-tion scores were similar between groups. There was astatistically significant difference in motor seizure dur-ation between groups (p = 0.048), with the lowest dur-ation measured in the dexmedetomidine 1 mcg/kggroup. However, post hoc analysis indicated no signifi-cant differences with p > 0.0167 with Bonferroni correc-tion; 0.05/3 pairs = 0.0167 (mean difference, − 9.208; 95%CI [− 20.9, 2.49]).
DiscussionThis study demonstrates that dexmedetomidine can at-tenuate the hemodynamic response after ECT. Eitherdexmedetomidine 0.5 mcg/kg or 1 mcg/kg attenuatedhypertension immediately after ECT for at least 30 min,the maximum length of time measured in this study.The two dexmedetomidine doses produced similar de-grees of blood pressure attenuation. However, only dex-medetomidine 1 mcg/kg decreased the tachycardiaresponse compared to the control group, as indicated inthe post hoc analysis. Dexmedetomidine administrationhad no statistically significant effect on recovery time,quality of ECT or motor and EEG seizure durations.Asystole duration, a complication after ECT, was alsonot affected by the drug administration.Dexmedetomidine has been used in previous studies
to attenuate the hemodynamic response in stress situa-tions [13, 14]. In the ECT setting, dexmedetomidine hasdemonstrated various effects, which may be due to dif-ferent drug doses or anesthetic regimens used in thestudies [4–6, 11, 12]. In a previous study, Fu and White[4] demonstrated that a single 0.5 or 1 mcg/kg dose ofdexmedetomidine before induction of anesthesia failedto decrease the peak mean arterial blood pressure(MAP) and HR after ECT. However, the varying of pre-medication time of dexmedetomidine administration ineach patient was used in the study. Additionally, labeta-lol, which was used by all of the participants in theirstudy, might influence the results. Moshiri et al. [7] useddexmedetomidine 0.5 mcg/kg, alfentanil 10 mcg/kg andsaline in a cross-over study. They reported no differencein hemodynamic parameters between dexmedetomidineand saline. However, atropine was administered to allpatients for bradycardia prophylaxis after using succinyl-choline in their study, which might confound thehemodynamic effect of dexmedetomidine. In contrast,
Table 1 Patient demographics data
Patient characteristics Mean ± SD
Age (y) 44.83 ± 12.71
Weight (kg) 71.71 ± 19.23
Height (cm) 162.67 ± 8.27
BMI (kg/m2) 27.04 ± 7.13
Underlying N (%)
Bipolar disorder 3 (12.5%)
Schizophrenia 14 (58.33%)
Schizoaffective disorder 6 (25%)
Hypertension 5 (20.83%)
DM 4 (16.67%)
ASA status (II/III) 18 (75%)/6 (25%)
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the cross-over study from Begec et al. [5], which used ahigher dose of dexmedetomidine (1 mcg/kg), reported asignificant reduction in hyperdynamic response to ECT.Another randomized controlled trial from Bagle et al.[15] reported a smaller increase in MAP and HR withdexmedetomidine 0.5 mcg/kg compared with saline. Alower dose of dexmedetomidine (0.2 mcg/kg) used in arandomized control trial by Li et al. [12] also produced asignificant reduction in HR and MAP compared with sa-line without altering seizure duration and recovery time.In the present study, we used dexmedetomidine 0.5mcg/kg and 1 mcg/kg, and expected the same benefit
with the two different doses, but fewer side effects withthe lower dose, which would also be more cost-effective.We limited the confounding factors by avoiding the useof any beta-blocker or anti-cholinergic drugs in thestudy protocol.Postictal asystole after ECT has been previously re-
ported [16–18]. The proposed mechanism is the un-opposed potent vagal stimulation by mechanoreceptorsafter ventricular systole from depleted catecholamines[16]. Dexmedetomidine has been shown to depress sinusand atrioventricular node function [19]. It may potenti-ate or attenuate postictal asystole risk; therefore,
Fig. 2 Blood pressure change in three group at different time points: dexmedetomidine 0.5 mcg/kg ( ), dexmedetomidine 1 mcg/kg
( ), normal saline ( ) BP (mmHg)
Fig. 3 Heart rate change in three group at different time points: dexmedetomidine 0.5 mcg/kg ( ), dexmedetomidine 1 mcg/kg ( ),
normal saline ( ) HR (beat per min)
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postictal asystole duration is an important outcome toconsider. Our study results were consistent with thecross-over study by Parikh et al. [11], which reportedthat dexmedetomidine 1 mcg/kg or dexmedetomidine0.5 mcg/kg and esmolol significantly ameliorated thecardiovascular response to ECT without affecting seizureduration. From our study, the best hemodynamic effectwas demonstrated in the dexmedetomidine 1 mcg/kggroup. Moreover, our study showed that this cardiovas-cular effect can last as long as 30 min after ECT, whichhas not been previously reported. The peak hyperdy-namic effect from ECT was observed at 2.5 to 5 minafter stimulation, with the peak HR occurring earlierthan the peak blood pressure. This may be explained bythe non-invasive blood pressure measurements that taketime to perform, whereas HR measurements were takenfrom real time electrocardiogram monitoring. Futurestudies using real time blood pressure monitoring, suchas intraarterial blood pressure, should be considered toconfirm the result. However, dexmedetomidine 0.5 mcg/kg failed to attenuate the peak HR response at 2.5 minafter ECT compared with saline, as shown in Fig. 3.Motor seizure duration was decreased in the dexmede-
tomidine 0.5 mcg/kg and 1 mcg/kg groups comparedwith the control group. Motor seizure duration greaterthan 20–25 s is usually considered as adequate treatment[20]. We found that some of the patients in the dexme-detomidine 1 mcg/kg group had motor seizure durationsof less than 25 s, but none in the dexmedetomidine 0.5mcg/kg group. This result differs from the study by Par-ikh et al. and may affect the quality of ECT in our pa-tients. However, we also recorded EEG seizure duration,and EEG measures are modestly associated with clinicaloutcomes [21].Asystole is an uncommon but potentially fatal compli-
cation after ECT. Post-stimulus asystole occurs just afterelectrical stimulation, whereas postictal asystole occursjust after seizure-induced tachycardia stops [16]. Sharp,
unopposed vagal parasympathetic outflow during andimmediately after an electrical stimulus results in intensebut transient sinus bradycardia, with a period of sinusarrest [22]. Because of the sinus node and atrioventricu-lar nodal depression effect that has been reported afterdexmedetomidine administration [19], we were con-cerned that dexmedetomidine may increase the asystoleduration after the ECT stimulus. However, postictalasystole was not observed in the present study, and post-stimulus asystole with duration of 6 to 9 s was observed,but did not significantly differ between the groups.Recovery time was slightly longer in the dexmedetomi-
dine groups compared with the saline group, but thiswas not statistically or clinically significant. The recoverytime difference was between 5 to 10min. Although postECT agitation scores were similar between the groups,patients who received dexmedetomidine 1 mcg/kgseemed to be calmer and less agitated; most of the pa-tients had an agitation score of 1 and none had agitationscores of 3–4. This favorable result is similar to manyprevious studies [7, 11, 23, 24].This study had a few strengths and limitations that
were worth noting. The study’s strengths were that itwas a crossover, double-blind randomized controlledtrial with no other medications interfering with theresults of the study, such as beta-blockers or atropine.However, it is necessary to note that this study was asingle-center clinical trial with a limited sample size.Multicenter or psychiatric disease-specific studies withlarger sample sizes should be considered. Additionally,all of the patients in this study had previously re-ceived an ECT treatment course. We did not limitthe induction agents depending on individualized ef-fective regimens use before the study began, so pa-tients received thiopental, propofol, or a combination.This may affect seizure duration measurements, aspropofol produces shorter seizure times comparedwith thiopental [25].
Table 2 Secondary outcomes compare in three groups
DEX0.5(n = 24)
DEX1.0(n = 24)
NSS(n = 24)
P-value
ECT Energy (J)a 55 (40–72.5) 55 (37.5–85) 55 (35–70) 0.762
Data presented as mean ± standard deviation, amedian (interquartile range), bn (%)
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ConclusionDexmedetomidine 1 mcg/kg administered 15min beforeECT attenuated the hemodynamic response, includingsuppressing the systolic, diastolic and HR increases, dur-ing ECT without affecting recovery time. It also did notprolong the post-stimulus asystole duration. However,motor seizure duration was slightly shorter with thisdexmedetomidine dose than with the 0.5 mcg/kg doseor saline, which may affect the quality of ECT. Decreas-ing the dexmedetomidine dose to 0.5 mcg/kg improvedmotor seizure duration compared with dexmedetomi-dine 1 mcg/kg, but also decreased the degree ofhemodynamic attenuation.
AbbreviationsASA: American Society of Anesthesiologist; BMI: Body mass index;DEX: Dexmedetomidine; DM: Diabetes mellitus; ECT: Electroconvulsivetherapy; EEG: Electroencephalogram; HR: Heart rate; MAP: Mean arterialblood pressure; NSS: Normal saline; SBP: Systolic blood pressure;DBP: Diastolic blood pressure
AcknowledgmentsThe authors acknowledge Assist. Prof Sunthiti Morakul and Lesley McCollum,PhD, from Edanz Group for language editing.
Authors’ contributionsAll authors were responsible for the conception and design of the study. PSdesigned and conducted the study, analyzed data, searched the literature,and wrote the manuscript. VL helped to supervise the study and gave acritical review of the study. PW and PI helped to conduct the study, searchliterature, and revised the manuscript. AL helped to conduct the study,collect, analyze and interpret data and draft the manuscript. SL helped tocollect the data. All authors have read and approved the final manuscript.
FundingThis study was funded by Ramathibodi Hospital, Mahidol University, Thailand.This study received no specific grant from any funding agency in thecommercial sector.
Availability of data and materialsThe datasets used and analyzed during the current study are available fromthe corresponding author upon reasonable request.
Declarations
Ethics approval and consent to participateThe study was approved by the Ethics Committee of Faculty of MedicineRamathibodi Hospital, Mahidol University, Bangkok, Thailand, ChairpersonAsst. Prof. Chusak Okascharoen, EC number 02–60-15 on May 4, 2017.Written informed consent was obtained from all participants.
Consent for publicationNot applicable.
Competing interestsThe authors declare that they have no competing interests.
Author details1Department of Anesthesiology, Faculty of Medicine Ramathibodi Hospital,Mahidol University, Bangkok, Thailand. 2Department of Psychiatry, Faculty ofMedicine Ramathibodi Hospital, Mahidol University, 270 Rama VI Road,Rachathewi, Bangkok 10400, Thailand.
Received: 30 April 2021 Accepted: 27 July 2021
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